An Evaluation of Palladin Overexpression in Pancreatic Cancer Cells

Abstract

Pancreatic cancer (PC) is the fourth leading cause of cancer in United States with overall survival rates of less than 5% (ACS, 2018). Its aggressive nature and late onset of physical symptoms lead to poor prognoses. Recognition of biomarkers is clearly an imperative undertaking for the disease. To tackle this problem, we evaluated the secreted protein profile of pancreatic cancer cell lines derived from different stages. In total, nine human pancreatic cancer cell lines were successfully adapted into serum‐free environments from which conditioned media was collected by a combination of ultracentrifugation, molecular weight cutoff, protein precipitation, gel‐based separation, and tryptic digestion followed by mass spectrometry protein identification. A small subset of proteins has been identified and validated biochemically including Palladin (PALLD), a pancreatic cancer susceptibility protein shown to be up‐regulated in previous studies. PALLD is a scaffolding protein that supports remodeling of the actin cytoskeleton in association with integrins at focal adhesion sites to coordinate cell migration. We demonstrate a possible interaction between PALLD and the beta5 integrin (ITGB5) indicative of the increased motile phenotype in PC. Taken together, our results suggest that PALLD overexpression is associated with enhanced motility in pancreatic cancer cells and could represent a potential biomarker or therapeutic strategy against pancreatic cancer progression.Support or Funding InformationThis work was funded in part through intramural programs at Fresno State to KV, RCB, JAB, and through NCI P20CA138025 to JAB.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.